pre-existing conditions

Question 1

pregestational and gestational diabetes

Answer 1

hyperglycemia resulting from defects in insulin secretion, insulin action, or both. pregestational diabetes is diabetes 1 (B-cell destruction in pancreas) or 2 (insulin resistance or deficiency) that was present in women before pregnancy. gestational diabetes is women who have carbohydrate intolerance discovered during pregnancy - any degree of glucose intolerance with onset or recognition during pregnancy; applies whether insulin used for treatment or diabetes persists after pregnancy. Women who experience gestational diabetes should be followed up with 6 weeks and 6 months after birth for presence of underlying disease

Question 2

signs of diabetes in pregnancy

Answer 2

polyuria - large volumes of urine due to kidney excreting excess blood volume from hyperglycemia (hyperglycemia causes hyperosmolarity where intracellular fluid gets pulled into the vascular system to dilute the glucose concentration)
glycosuria - glucose in the urine
polydipsia - excessive thirst due to polyuria and cellular dehydration
polyphagia - excessive hunger caused by starvation due to tissue breakdown of fats and muscles for energy to compensate for inability of body to convert carbs (glucose) into energy

Question 3

two insulin conditions in diabetes

Answer 3

impaired insulin secretion due to beta cells of the pancreas being destroyed by an autoimmune process
inadequate insulin action in target tissues at one or more points along the metabolic pathway
- both these conditions present in same person, difficult to determine which abnormality is primary

Question 4

normal glucose cycle in pregnancy

Answer 4

glucose, primary fuel used by the fetus, is transported across the placenta through diffusion, thus glucose level in fetus directly proportional to maternal glucose level. Glucose crosses the placenta but insulin does not so around the 10th week the fetus secretes its own insulin level to match the glucose level crossing the placenta. in first and second trimester Estrogen and progesterone (pregnancy hormones) stimulate the B-cells in the pancreas to increase insulin production; increasing peripheral use of glucose and decreasing blood glucose. At the same time increases in tissue glycogen stores and decrease in hepatic glucose production lower fasting glucose. During latter part of second and all through third trimester pregnancy exerts a diabetogenic effect, decreasing tolerance of glucose, increasing insulin resistance, decreasing hepatic stores, and increasing hepatic production of glucose. insulin resistance is a glucose sparing mechanism to ensure enough glucose for the fetus. Insulin requirements increase from 18 or 24 weeks to 36 weeks where it levels out. at birth the expulsion of the placenta prompts an abrupt decrease in pregnancy hormones, cortisol, and insulinase. maternal tissue quickly regains its prepregnancy sensitivity to insulin. for non breastfeeding it prepregnancy insulin-carb balance restored in 7 to 10 days. in breastfeeding insulin requirement remains low until infant weaned.

Question 5

pregestational diabetes and glucose levels in pregnancy

Answer 5

due to low glucose level as natural part of first and second trimester women with pregestational diabetes tend to be hypoglycemic. women with diabetes require insulin throughout pregnancy. Hormonal changes in pregnancy that affect glycemic control may accelerate vascular complications of diabetes. During first semester when blood glucose is low and insulin response to glucose is enhanced there is better glycemic control. Insulin dose must be adjusted during pregnancy for rising insulin resistance in second and third trimester (more insulin needed) and and hypoglycemia in first and second trimester (less insulin needed).

Question 6

preconception counselling for diabetic women

Answer 6

strict metabolic control important to reduce congenital anomalies and spontaneous abortion during organogenesis in early weeks of pregnancy. use of oral antihyperglycemic meds alone in pregnancy not recommended.

Question 7

Maternal risks with diabetes in pregnancy

Answer 7

risk factors include blood glucose control, length of time since diagnosis, and existing diabetic complications present. women with pregestational diabetes who have poor glycemic control (defined as glycosylated hemoglobin value greater than 7.0% around time of conception and in early pregnancy) have twofold increased incidence of early pregnancy loss. Poor glycemic control later in pregnancy increase the rate of fetal macrosomia (birth weight more than 400-4500g). assessment for retinopathy recommended in preconception, during first trimester, as needed throughout pregnancy, and 1 year postpartum. Hydramnios (Amniotic fluid index (AFI) greater than 24 and 25cm) frequently develop during third trimester of woman with diabetes thought to result from increase glucose concentration in amniotic fluid from maternal and fetal hyperglycemia.

Question 8

infection in diabetic pregnant woman

Answer 8

disorder of carbohydrate metabolism alter body’s normal resistance to infection - inflammation response, leukocyte function, and vaginal pH all affected. infection may cause insulin resistance resulting in ketoacidosis. postpartum infection more likely to occur in woman with poor glycemic control. Most common concern in pregnancy is loss of hypoglycemic awareness - more common in long standing diabetes and safety concern for mothers- hypoglycemic awareness may return after pregnancy.

Question 9

ketoacidosis in pregnancy

Answer 9

build up of ketones in the blood due to hyperglycemia - the body breaks down fat too fast to accommodate for energy demands and releases ketones into the blood making it more acidic; leads to metabolic acidosis. occurs most often during second and third trimester when diabetogenic effect is greatest. DKA occur due to over or under administration of insulin. DKA occur with blood glucose levels barely exceeding 11 mmol/L because of increase in the body’s resistance to insulin. Excessive blood glucose and ketones results in osmotic diuresis with subsequent loss of fluids and electrolytes, volume depletion, and cellular dehydration.

Question 10

Hypoglycemia in diabetic pregnancy

Answer 10

less than normal amount of glucose in the blood. Abnormal postnatal neurological development occurs when long term hypoglycemia results in ketosis (break down of fat or muscle to meet energy demands not provided by carbs - glucose)

Question 11

fetal and neonatal risks with diabetes

Answer 11

stillbirth significant risk. in third trimester fetal acidosis is most likely cause of death. most important cause of perinatal loss is congenital malformation - incidence of malformations directly related to severity and duration of diabetes. Hyperglycemia during organogenesis main cause of birth defects. Morbidity and mortality of fetal reduce with strict maternal glycemic control before and during pregnancy. Macrosomia due to increased insulin secretion (hyperinsulinism) to accommodate hyperglycemia acting as a growth hormone. Hypoglycemia also risk for infants depending on glycemic control of mother in last trimester of pregnancy (increased insulin demands)

Question 12

insulin shock (hypoglycemia) in pregnancy

Answer 12

due to: excess insulin, insufficient food (delayed or missed meals), excessive excersize or work, indigestion (vomiting or diarrhea). Rapid onset for regular insulin or gradual onset for modified insulin or oral hypoglycemic agents. s&s: hunger, blurred vision, personality changes,

Question 13

interventions for insulin shock in pregnancy

Answer 13

check blood glucose levels, eat 15g of fast sugar, recheck blood glucose in 15min and eat another 15g fast sugar if low, recheck blood glucose in 15min again, notify healthcare provider if no change in blood glucose level. If woman unconscious admin 50% dextrose IV push, 50 to 10% dextrose in water IV drip, or 1 mg glucagon subQ. obtain blood and urine specimen for lab testing

Question 14

diabetic ketoacidosis (hyperglycemia) in pregnancy

Answer 14

due to: insufficient insulin, excess or wrong kind of food, infection, injury, or illness, emotional stress, insufficient excersize. Slow onset (hours to days). S&S: thirst, abdominal pain, acetone (fruity) breath odour

Question 15

interventions for DKA in pregnancy

Answer 15

notify healthcare provider, admin insulin in accordance with blood glucose levels, give IV fluids such as normal saline solution or one half normal saline solution; potassium when urinary output adequate; bicarbonate for pH <7, monitor laboratory testing of blood and urine

Question 16

hyperthyroidism in pregnancy

Answer 16

most commonly caused by graves disease or human chorionic gonadotropin (hCG) mediated hyperthyroidism. symptoms generally begin 4 to 8 weeks of gestation and involve severe nausea and vomiting. dx: thyroid levels in blood. woman with minimal or mild symptoms - low thyroid stimulating hormone and mild elevated thyroxine - can be monitored without intervention. Signs to differentiate mild from severe hyperthyroidism include unplanned weight loss, loose nails, and HR 100bpm/min or higher. two primary meds to treat hyperthyroidism in pregnancy; propylthiouracil (PTU) and methimazole (MM). MM has teratogenic effects so is avoided in first trimester, PTU is associated with liver failure so only used in first trimester to prevent toxicity. Thyroid function test performed 2 to 4 weeks after switch from PTU to MM to be sure euthyroid maintained. Beta adrenergic blockers used for severe symptoms but not long term due to adverse effects on postnatal bradycardia, anoxic stress, hypoglycemia, and IUGR. med can be passed through breastfeeding so a breastfeeding newborn thyroid function should be monitored periodically to prevent hypothyroidism. In severe cases, hyperthyroidism can be surgically dealt with by removing the thyroid (subtotal thyroidectomy) in second or third trimester.

Question 17

thyroid storm in pregnancy

Answer 17

uncommon but serious complication of untreated or partially treated hyperthyroidism. it occurs in response to stresses such as severe pre-eclampsia, infection, birth or surgery. Prompt treatment with PTU, IV fluids, and oxygen required. Potassium iodide, antipyretics, glucocorticoids, and beta adrenergic blockers may also be given; sedation may be necessary. symptoms include sudden fever, tachycardia, restlessness, vomiting, hypotension, or stupor. HF also may occur

Question 18

hypothyroidism in pregnancy

Answer 18

TSH levels high caused by underactive thyroid. most common cause of thyroid problems is iodine deficiency. signs of hypothyroidism include cool and dry skin, weight gain, coarsened hair, muscle weakness, cold intolerance, decrease in excersize capacity, constipation, and fatigue. hypothyroidism shown to cause neurological development impairment in early fetal development. fetus dependent on maternal transfer of thyroid hormones for first 18 weeks of pregnancy, specifically T4 - if mother deficient, fetal brain cannot develop properly. Thyroid hormone supplement treatment of choice, specifically levothyroxine as it is not a teratogenic. Thyroid hormone treatment must be adjustment for demand throughout pregnancy (demand generally goes up as pregnancy progresses). Take meds on empty stomach for increased absorption and take prenatal vitamins 4 hours after thyroid hormones as iron and calcium affect absorption of hormone.

Question 19

Maternal cardiac disease risk group 1

Answer 19

mortality rate <1%
ASD and VSD
PDA
corrected tetralogy of fallot
pulmonic/tricuspid disease
mitral stenosis or aortic regurgitation
bioprosthetic valve
mitral valve prolapsed with regurgitation

Question 20

maternal cardiac disease risk group 2

Answer 20

mortality rate 5-20%
aortic stenosis
coarctation of the aorta without valve involvement
artificial heart valves
mitral stenosis or with atrial fibrillation
uncorrected tetralogy of fallot
previous myocardial infarction
marfan syndrome with normal aorta

Question 21

maternal cardiac disease risk group 3

Answer 21

mortality rate 25-50%
pulmonary hypertension
coarctation of the aorta with valvular involvement
complicated marfan syndrome with aortic involvement
endocarditis
eisenmenger syndrome
peripartum cardiomyopathy with persistent left ventricular dysfunction

Question 22

Cardiovascular disorders in pregnancy

Answer 22

changes that occur in pregnancy that affect women with cardiac disease are increased vascular volume, decreased systemic vascular resistance, cardiac output changes in labour, and intravascular changes that occur just after birth
if myocardial disease develops, valvular disease exists, or congenital heart defect is present, cardiac decompensation (inability of the heart to maintain a sufficient cardiac output) may occur
Fever and infection major causes of cardiac decompensation in pregnancy

Question 23

New York Heart Association (NYHA) functional classification of heart disease

Answer 23

Class I: asymptomatic without limitation of physical activity
Class II: symptomatic with slight limitation of activity
Class III: symptomatic with marked limitation of activity
Class IV: symptomatic with inability to carry out activity without discomfort
note: woman assessed for classification at 3 months and then again at 7 or 8 months

Question 24

congenital cardiac disease in pregnancy

Answer 24

women at risk for cardiac event in pregnancy include those with a prior cardiac event, arrhythmia, NYHA functional class greater than II, cyanosis, left heart obstruction, and systemic ventricular dysfunction

Question 25

ASD in pregnancy

Answer 25

tends to be asymptomatic. most common CHD seen in pregnancy. usually uncomplicated pregnancy but some woman can develop heart failure or arrhythmias as a result of increased blood volume. another possible complication is emboli (blood clot)

Question 26

VSD in pregnancy

Answer 26

not commonly seen in pregnancy due to fixing earlier in life. Uncomplicated pregnancy with minor VSD. if defect is large risk of heart failure or pulmonary hypertension. tx: anticoagulants and rest

Question 27

PDA in pregnancy

Answer 27

generally fixed earlier in life. Small PDA minor or few complications. Large PDA that results in increased left to right shunting results in hemodynamic changes that evolve to eisenmenger syndrome which is fatal to mother and fetus - recommended termination

Question 28

coarctation of the aorta in pregnancy

Answer 28

uncorrected coarctation of the aorta is relatively safe during pregnancy. tx: rest and antihypertensive medications - preferably beta adrenergic blocking agents. Some recommendations for C birth to prevent blood pressure elevation during second stage labour that could lead to rupture of vessels or aorta
if bacteremia suspected - prophylactic antibiotics given during labour

Question 29

marfan syndrome in pregnancy

Answer 29

marfan syndrome - autosomal dominant condition of generalized weakness of connective tissue, resulting in characteristic feature of the disease, aortic wall and root dilation. S&S: dislocation of optic lens, deformity of anterior thorax, scoliosis, long limbs, joint laxity, and arachnodactyly (spidery fingers)
mortality rate as high as 50% - however, is aortic root dilation of 40mm or less, mortality less than 5%
repair of aortic root recommended if diameter 5.5 to 6cm before pregnancy, if root less than 4cm can attempt pregnancy with modest risk
tx: limited physical activity, prevention of hypertensive or hypotensive complications, admin of beta blockers as needed to maintain resting HR of 70bpm, and tachycardia prevention in labour

Question 30

tetralogy of fallot in pregnancy

Answer 30

most common cyanotic heart disease seen in pregnancy (ASD most common acyanotic). components of TOF: pulmonary stenosis, VSD, overriding aorta, and right ventricle hypertrophy - right to left shunting. Surgical correction recommended as patched VSD and repaired pulmonary stenosis results in pregnancy with no significant risk. With uncorrected FOT right to left shunting results in reduced pulmonary blood flow and increasing hypoxemia, which can cause syncope (fainting) and death.
tx: maintenance of venous return critical in TOF therefore most dangerous time is third trimester and postpartum - when venous return reduced by large uterus and peripheral blood pooling after birth; blood volume must be adequately maintained. Prophylactic antibiotics given intrapartum period, pressure graded support hose recommended

Question 31

Eisenmenger syndrome in pregnancy

Answer 31

right to left or bidirectional shunting that can be at atrial or ventricular level and is combined with elevated pulmonary vascular resistance. Associated with underlying structural defect like VSD (most common) or PDA. high risk means pregnancy avoided or terminated in these women. Death can occur at any time but intrapartum and early postpartum period most common.
maternal morbidity: right ventricular failure and associated cardiogenic shock
tx: measures to maintain pulmonary blood flow, physical activity limited, pressure graded elastic support hose, oxygen therapy
during labour tx: narcotic based anesthesia provide pain relief without causing excessive hemodynamic instability
hypotension prevented at all cost bc it results in more right to left shunting, increasing hypoxemia, increasing pulmonary resistance, and worsening shunt. Volume overload or excessive systemic resistance prevented to stop further stress of the failing right side of the heart

Question 32

primary pulmonary hypertension in pregnancy

Answer 32

constriction of the arteriolar vessels in the lung, leading to increased pulmonary artery pressure- results in right ventricular hypertension, right ventricular hypertrophy with tricuspid regurgitation and systemic congestion. Pregnancy not advised with this condition. most dangerous time is intrapartum and early postpartum period bc of increased cardiac output and fluid shifts.
tx: limiting activity and avoiding supine position, diuretics, supplemental oxygen, and vasodilator meds
during labour: hypotension must be avoided by carefully establishing epidural analgesia and preventing blood loss - hypotension impairs ability of right ventricle to pump blood through pulmonary veins due to their high fixed resistance

Question 33

mitral valve stenosis in pregnancy

Answer 33

always caused by rheumatic heart disease (RHD). mitral valve stenosis - narrowing of the opening of the mitral valve caused by stiffening valve leaflets - causes obstruction of the blood flow from the atrium to the ventricles.
tight stenosis plus increase blood volume and cardiac output of pregnancy may cause complications in pregnancy
maternal mortality related to functional capacity - women with mild to moderate stenosis tolerate pregnancy well (NYHA classification III or IV associated with maternal deaths)
prevention: daily oral penicillin G or monthly penicillin benzathine if increased risk of exposure to streptococcal infection in pregnancy
tx: diuretics such as furosemide to prevent pulmonary edema and beta blockers or calcium channel blockers to prevent tachycardia, cardioversion for new onset atrial fibrillation, chronic atrial fibrillation need digoxin or beta blockers to control HR, anticoagulant therapy to prevent embolism, reduced activity, restricting dietary sodium, and bedrest. Prophylaxis antibiotics for intrapartum endocarditis and pulmonary infection
intrapartum care for severe disease: invasive hemodynamic monitoring during labour - goal to maintain adequate ventricular filling and cardiac output, give birth in lateral decubitus position, shortening second stage of labour with vacuum or forceps (to decrease cardiac workload)
surgical intervention necessary during pregnancy if medical therapy not effective - valve replacement and open commissurotomy or balloon valvotomy (preferred)

Question 34

aortic stenosis in pregnancy

Answer 34

medical management same for mitral stenosis

rarely encountered as generally occurs after childbearing years

Question 35

mitral valve prolapse in pregnancy

Answer 35

common, benign condition. mitral valve leaflets prolapse into left atrium during ventricular systole, allowing some backflow of blood. generally asymptomatic, chest pain sometimes felt - give beta blocking drugs - if severe check thyroid function. antibiotic prophylaxis for invasive procedure and complicated vaginal birth

Question 36

oxytocin after pregnancy

Answer 36

Dilute IV oxytocin immediately after birth may be used to

prevent hemorrhage. also used for induction of labour - causes uterine contractions

Question 37

anemia in pregnancy

Answer 37

reduction of the oxygen carrying capacity of the blood; heart tries to compensate by increasing the cardiac output - increased cardiac workload and stresses ventricular function. Anemia occurring with any other complication can result in HF.
hydremia - dilution of blood; pregnancy increases blood volume by 50% resulting in dilution of oxygen carrying RBC; also called physiological anemia of pregnancy
anemia in pregnancy - hematocrit level 0.32 or lower
when a woman have anemia during pregnancy, loss of blood at birth is not well tolerated - increased risk for blood transfusion.

Question 38

iron deficiency anemia in pregnancy

Answer 38

most common form of anemia. iron transported across placenta for fetal erythropoiesis. treatment through diet, oral supplement, prophylactic iron supplement, and if oral supplement not tolerated iron sucrose or iron dextran (parenteral iron)
iron sucrose preferred

Question 39

sickle cell hemoglobinopathy in pregnancy

Answer 39

women with sickle cell anemia high risk of developing stroke, pre-eclampsia, HF, cardiomyopathy, pyelonephritis, leg ulcers, and bone abnormalities. Encouraged to take low dose aspirin after first trimester to reduce risk pre-eclampsia. Crises managed with hydration, oxygen, and analgesia.

Question 40

asthma in pregnancy

Answer 40

increased risk of hemorrhage and pre-eclampsia. If excessive bleeding occurs, prostaglandin E2 or E1 given - pt respiratory status monitored

Question 41

bells palsy in pregnancy

Answer 41

unilateral weakness of the face, max weakness 48 hrs after onset, pain surround ear, eye cannot close completely, loss of taste and hyperacusis.
Cause unknown, thought to occur due to HIV or herpes virus. Increase risk of gestational hypertension. steroids 5 to 6 days after paralysis thought to be helpful. tx: prevention of injury to exposed cornea, facial muscle massage, careful chewing and removal of food in paralyzed cheek, and reassurance

Question 42

HIV and AIDS in pregnancy

Answer 42

ART decreases perinatal transmission rates and progression to AIDS. Preconception counselling should include HIV history, current physical status, and prenatal and HIV specific lab results. Care in pregnancy include strict adherence with ART regimen, follow through with regular HIV specific blood level monitoring (viral plasma levels and immune function), and education regarding labour, birth, and postpartum. Perinatal transmission of HIV can occur in the first trimester through maternal blood circulation, to the infant during labour, or through breastmilk.

Question 43

Factors increasing risk of mother infant HIV transmission

Answer 43

lack of maternal and infant treatment with ART and prevention
maternal plasma viral level greater than 1000 copies per milliliter
maternal vaginal infection during pregnancy
amniocentesis, chorionic villus sampling, or both
ruptured membranes
presence of chorioamnionitis
fetal scalp monitoring and venous scalp sampling
interventions such as forceps, vacuum, and external cephalic version
breastfeeding

Question 44

obstetrical complications of HIV in pregnancy

Answer 44

Many variables (poverty, drug use, mental health issues, etc) can account for a woman being at risk for preterm labour and birth, premature rupture of membranes, perinatal loss, and IUGR. The mode of birth for women who are HIV positive depends on the woman’s plasma viral level and her status of labour upon admission. If a woman’s plasma level is less than 1000 copies per millilitre and she has
received ART, she can proceed with a vaginal birth. In women positive for HIV who are not receiving antiretrovirals and have a plasma load greater than 1000, an unknown plasma level, or antepartum bleeding, a Caesarean birth is recommended
The postpartum period for the woman infected with HIV may be notable for infection, hemorrhage, or both
HIV-related thrombocytopenia may also increase the risk of
hemorrhage. It is critical that women remain on their antiretroviral medication throughout their pregnancy and into the postpartum period.

Question 45

HIV nursing care in pregnancy

Answer 45

All HIV-infected women should be treated with ART during
pregnancy, regardless of the CD4 counts. ART should include
three drugs from at least two classes of antiretroviral medications
The major adverse effect of these medications is bone marrow suppression
IV zidovudine is administered to the HIV-positive woman during the intrapartum period. A loading dose is initiated on her admission in labour, followed by a continuous maintenance dosage throughout labour
Increased duration of ruptured amniotic membranes has been associated with increased perinatal transmission - If rupture of membranes occurs before labour, induction of uterine contractions with oxytocin
Immediately after birth, infants should be wiped free of all body fluids. Prior to blood testing or any injections, the skin area should be cleansed well with soap and water
Oral zidovudine treatment for the infant is initiated within 6 hours of life and continues for up 6 weeks